Most neuronal models of addiction identify networks specific to motivation (craving) and cognitive control. The central concern during treatment of drug dependence is the return to drug use after periods of abstinence; this likely involves varying degrees of (dys)function within these neuronal networks. Neurostimulation techniques such as transcranial direct current stimulation (tDCS) have been used as interventions for substance use disorders. tDCS may have promise as adjuvant treatment for buprenorphine initiators because considerable work on addictive substances other than opioids suggests treatment targeted at the dorsolateral prefrontal cortex (DLPFC; region involved in self-regulation) may reduce craving and drug consumption. One critique of tDCS has been lack of evidence that brain stimulation changes targeted cognitive control and motivation networks. Functional magnetic resonance imaging (FMRI) may help bridge this gap and identify clinically meaningful changes in both networks post tDCS treatment. In addition, examining neurophysiological indicators that could confirm the effect of tDCS on the DLPFC is an innovative approach to furthering our understanding of the potential for neurostimulation to disrupt the addictive process and reduce relapse risk among those with OUD. The DLPFC has shown to be a spatially selective stimulation target for tDCS enhancement of working memory. Working memory requires inputs from a number of cortical and subcortial regions, and involves a complex series of processes that are associated with charactristic electroencephalographic (EEG)signals during performance of computer-based tasks like the n-back. Specifically, frontal theta activity on EEG during WM tasks comprises a quantifiable oscillatory target for engagement and modulation. Therefore, if this signal increases with tDCS, it is suggestive that the DLPFC has been modulated with active stimulation. In our currently NIDA-funded UG3 DA047793, ?tDCS to Decrease Opioid Relapse?, we will measure behavioral and brain responses following tDCS stimulation to the DLPFC delivered during cognitive control network (CCN) priming and utilizing FMRI. In this administrative supplement, we propose to include an additional validation measure of the effect of tDCS on the DLPFC ? an oscillatory target -- EEG frontal theta power during WM. As such, the Go/no go criteria for the UH3 phase will be demonstration of significant effects of active tDCS (versus sham stimulation) as: (a1) FMRI change in any node of the CR or CCN networks OR (a2) enhanced frontal theta power during an WM task, AND (b1) reduced subjective craving measured post-treatment (outside FMRI scan) OR (b2) reduced craving during an FMRI cue reactivity task. !